Data needs for hyperspectral detection of algal bloom diversity across the globe.

A group of 38 experts specializing in hyperspectral remote-sensing methods for aquatic ecosystems attended an interactive Euromarine Foresight Workshop at the Flanders Marine Institute (VLIZ) in Ostend, Belgium, June 4–6, 2019. The objective of this workshop was to develop recommendations for comprehensive, efficient, and effective laboratory and field programs to supply data for development of algorithms and validation of hyperspectral satellite imagery for micro-, macro- and endosymbiotic algal characterization across the globe. The international group of researchers from Europe, Asia, Australia, and North and South America (see online Supplementary Materials) tackled how to develop global databases that merge hyperspectral optics and phytoplankton group composition to support the next generation of hyperspectral satellites for assessing biodiversity in the ocean and in food webs and for detecting water quality issues such as harmful algal blooms. Through stimulating discussions in breakout groups, the team formulated a host of diverse programmatic recommendations on topics such as how to better integrate optics into phytoplankton monitoring programs; approaches to validating phytoplankton composition with ocean color measurements and satellite imagery; new database specifications that match optical data with phytoplankton composition data; requirements for new instrumentation that can be implemented on floats, moorings, drones, and other platforms; and the development of international task forces. Because in situ observations of phytoplankton biogeography and abundance are scarce, and many vast oceanic regions are too remote to be routinely monitored, satellite observations are required to fully comprehend the diversity of micro-, macro-, and endosymbiotic algae and any variability due to climate change. Ocean color remote sensing that provides regular synoptic monitoring of aquatic ecosystems is an excellent tool for assessing biodiversity and abundance of phytoplankton and algae in aquatic ecosystems. However, neither the spatial, temporal, nor spectral resolution of the current ocean color missions are sufficient to characterize phytoplankton community composition adequately. The near-daily overpasses from ocean color satellites are useful for detecting the presence of blooms, but the spatial resolution is often too coarse to assess the patchy distribution of blooms, and the multiband spectral resolution is generally insufficient to identify different types of phytoplankton from each other, even if progress has undeniably been achieved during the last two decades (e.g., IOCGG, 2014). Moreover, the methods developed for multichannel sensor use are often highly tuned to a region but are inaccurate when applied broadly. New orbital imaging spectrometers are being developed that cover the full visible and near-infrared spectrum with a large number of narrow bands dubbed “hyperspectral” (e.g., TROPOMI, PRISMA, EnMAP, PACE, CHIME, SBG). Hyper-spectral methods have been explored for many years to assess phytoplankton groups and map seafloor habitats. However, the utility of hyperspectral imaging still needs to be demonstrated across diverse aquatic regimes. Aquatic applications of hyperspectral imagery have been limited by both the technology and the ability to validate products. Some of the past hyperspectral space-based sensors have suffered from calibration artifacts, low sensitivity in aquatic ecosystems (e.g., CHRIS, HICO), and very low spatial resolution (e.g., SCIAMACHY), but the next generation of sensors are planned to have high signal-to-noise ratio and improved performance over aquatic targets. Providing data to develop and validate hyperspectral approaches to characterize phytoplankton groups across the globe poses new challenges. Several recent studies have documented gaps that need to be filled in order to assess algal diversity across the globe (IOCCG, 2014; Mouw et al., 2015; Bracher et al., 2017), which promoted/inspired the formation of this workshop

Extending Landsat 8: Retrieval of an Orange contra-Band for Inland Water Quality Applications

The Operational Land Imager (OLI) onboard Landsat 8 has found successful application in inland and coastal water remote sensing. Its radiometric specification and high spatial resolution allows quantification of water-leaving radiance while resolving small water bodies. However, its limited multispectral band set restricts the range of water quality parameters that can be retrieved. Identification of cyanobacteria biomass has been demonstrated for sensors with a band centered near 620 nm, the absorption peak of the diagnostic pigment phycocyanin. While OLI lacks such a band in the orange region, superposition of the available multispectral and panchromatic bands suggests that it can be calculated by a scaled difference. A set of 428 in situ spectra acquired in diverse lakes in Belgium and The Netherlands was used to develop and test an orange contra-band retrieval algorithm, achieving a mean absolute percentage error of 5.39 % and a bias of −0.88 % in the presence of sensor noise. Atmospheric compensation error propagated to the orange contra-band was observed to maintain about the same magnitude (13 % higher) observed for the red band and thus results in minimal additional effects for possible base line subtraction or band ratio algorithms for phycocyanin estimation. Generality of the algorithm for different reflectance shapes was tested against a set of published average coastal and inland Optical Water Types, showing robust retrieval for all but relatively clear water types (Secchi disk depth > 6 m and chlorophyll a < 1.6 mg m−3). The algorithm was further validated with 79 matchups against the Ocean and Land Colour Imager (OLCI) orange band for 10 globally distributed lakes. The retrieved band is shown to convey information independent from the adjacent bands under variable phycocyanin concentrations. An example application using Landsat 8 imagery is provided for a knowncyanobacterialbloominLakeErie,US.ThemethodisdistributedintheACOLITEatmospheric correction code. The contra-band approach is generic and can be applied to other sensors with overlapping bands. Recommendations are also provided for development of future sensors with broad spectral bands with the objective to maximize the accuracy of possible spectral enhancement

DNA methylation map of mouse and human brain identifies target genes in Alzheimer’s disease

The central nervous system has a pattern of gene expression that is closely regulated with respect to functional and anatomical regions. DNA methylation is a major regulator of transcriptional activity, and aberrations in the distribution of this epigenetic mark may be involved in many neurological disorders, such as Alzheimer’s disease. Herein, we have analysed 12 distinct mouse brain regions according to their CpG 5’-end gene methylation patterns and observed their unique epigenetic landscapes. The DNA methylomes obtained from the cerebral cortex were used to identify aberrant DNA methylation changes that occurred in two mouse models of Alzheimer’s disease. We were able to translate these findings to patients with Alzheimer’s disease, identifying DNA methylation-associated silencing of three targets genes: thromboxane A2 receptor (TBXA2R), sorbin and SH3 domain containing 3 (SORBS3) and spectrin beta 4 (SPTBN4). These hypermethylation targets indicate that the cyclic AMP response element-binding protein (CREB) activation pathway and the axon initial segment could contribute to the disease

Alteration of inhibitory circuits in the somatosensory cortex of Ts65Dn mice, a model for Down's syndrome

Down's syndrome (DS), with an incidence of one in 800 live births, is the most common genetic disorder associated with mental retardation. This trisomy on chromosome 21 induces a variable phenotype in which the only common feature is the presence of mental retardation. The neural mechanisms underlying mental retardation might include defects in the formation of neuronal networks and neural plasticity. DS patients have alterations in the morphology, the density and the distribution of dendritic spines in the pyramidal neurons of the cortex. Our hypothesis is that the deficits in dendritic arborization observed in the principal neurons of DS patients and Ts65Dn mice (a model for DS that mimics most of the structural alterations observed in humans) may be mediated to some extent by changes in their inhibitory inputs. Different types of interneurons control different types of inhibition. Therefore, to understand well the changes in inhibition in DS, it is necessary to study the different types of interneurons separately. We have studied the expression of synaptophysin, Glutamic acid decarboxylase-67 (GAD-67) and calcium-binding protein-expressing cells in the primary somatosensory cortex of 4¿5 month old Ts65Dn mice. We have observed an increment of GAD67 immunoreactivity that is related mainly to an increment of calretinin-immunoreactive cells and among them the ones with bipolar morphology. Since there is a propensity for epilepsy in DS patients, this increase in interneurons might reflect an attempt by the system to block overexcitation rather than an increment in total inhibition and could explain the deficit in interneurons and principal cells observed in elderly DS patients

Clinical impact of HLA class I expression in rectal cancer

Contains fulltext : 69499.pdf (publisher's version ) (Open Access)PURPOSE: To determine the clinical impact of human leukocyte antigen (HLA) class I expression in irradiated and non-irradiated rectal carcinomas. EXPERIMENTAL DESIGN: Tumor samples in tissue micro array format were collected from 1,135 patients. HLA class I expression was assessed after immunohistochemical staining with two antibodies (HCA2 and HC10). RESULTS: Tumors were split into two groups: (1) tumors with >50% of tumor cells expressing HLA class I (high) and (2) tumors with < or =50% of tumor cells expressing HLA class I (low). No difference in distribution or prognosis of HLA class I expression was found between irradiated and non-irradiated patients. Patients with low expression of HLA class I (15% of all patients) showed an independent significantly worse prognosis with regard to overall survival and disease-free survival. HLA class I expression had no effect on cancer-specific survival or recurrence-free survival. CONCLUSIONS: Down-regulation of HLA class I in rectal cancer is associated with poor prognosis. In contrast to our results, previous reports on HLA class I expression in colorectal cancer described a large population of patients with HLA class I negative tumors, having a good prognosis. This difference might be explained by the fact that a large proportion of HLA negative colon tumors are microsatellite instable (MSI). MSI tumors are associated with a better prognosis than microsatellite stable (MSS). As rectal tumors are mainly MSS, our results suggest that it is both, oncogenic pathway and HLA class I expression, that dictates patient's prognosis in colorectal cancer. Therefore, to prevent confounding in future prognostic analysis on the impact of HLA expression in colorectal tumors, separate analysis of MSI and MSS tumors should be performed

E-cadherin transcriptional downregulation by promoter methylation but not mutation is related to epithelial-to-mesenchymal transition in breast cancer cell lines

Using genome-wide expression profiling of a panel of 27 human mammary cell lines with different mechanisms of E-cadherin inactivation, we evaluated the relationship between E-cadherin status and gene expression levels. Expression profiles of cell lines with E-cadherin (CDH1) promoter methylation were significantly different from those with CDH1 expression or, surprisingly, those with CDH1 truncating mutations. Furthermore, we found no significant differentially expressed genes between cell lines with wild-type and mutated CDH1. The expression profile complied with the fibroblastic morphology of the cell lines with promoter methylation, suggestive of epithelial-mesenchymal transition (EMT). All other lines, also the cases with CDH1 mutations, had epithelial features. Three non-tumorigenic mammary cell lines derived from normal breast epithelium also showed CDH1 promoter methylation, a fibroblastic phenotype and expression profile. We suggest that CDH1 promoter methylation, but not mutational inactivation, is part of an entire programme, resulting in EMT and increased invasiveness in breast cancer. The molecular events that are part of this programme can be inferred from the differentially expressed genes and include genes from the TGFbeta pathway, transcription factors involved in CDH1 regulation (i.e. ZFHX1B, SNAI2, but not SNAI1, TWIST), annexins, AP1/2 transcription factors and members of the actin and intermediate filament cytoskeleton organisation.Toxicolog

Разработка мероприятий по улучшению условий труда на примере предприятия ООО "Юргинский машиностроительный завод"

Abstract IL-6 is known to play a crucial role in the pathogenesis of chronic intestinal inflammation by modulating T cell functions. In this study, we investigated the role of gp130, the common signal transducer for all IL-6 cytokines, in a murine model of acute T cell independent colitis to better characterize the impact of gp130 on innate immune cells and the early stages of inflammation. Experimental colitis was induced by dextran sulfate sodium treatment of mice with inducible systemic deletion of gp130 (MxCre/gp130−/−), macrophage/neutrophil-specific gp130-deficiency (LysCre/gp130−/−), or bone marrow chimeric mice and compared with wild-type controls (gp130f/f). Systemic deletion of gp130 (MxCre/gp130−/−) protected mice from severe colitis and wasting and attenuated the mucosal inflammatory infiltrate as well as local cytokine, chemokine, and adhesion molecule expression. Experiments in newly generated macrophage/neutrophil-specific gp130-deleted animals (LysCre/gp130−/−) and gp130 bone marrow chimeric mice, revealed a dual mechanism of proinflammatory effects mediated by gp130. Leukocyte recruitment was impaired in gp130-deleted animals and gp130-deleted recipients of wild-type bone marrow, demonstrating a central role of gp130-dependent signals in nonmyeloid cells for directing leukocytes to sites of inflammation, which was further confirmed in a model of sterile peritonitis. In contrast, macrophage/neutrophil-specific gp130 deficiency delayed and attenuated the disease but only marginally affected the inflammatory infiltrate, indicating a defective activation of mucosal leukocytes. We provide evidence that IL-6 cytokines acting via gp130 are required in the acute stages of intestinal inflammation by modulating the dynamics of innate immune cell recruitment and activation.</jats:p

Changing Paradigms in Down Syndrome: The First International Conference of the Trisomy 21 Research Society

Down syndrome (DS) is the most common genetic cause of intellectual disability (ID) in humans with an incidence of ∼1:1,000 live births worldwide. It is caused by the presence of an extra copy of all or a segment of the long arm of human chromosome 21 (trisomy 21). People with DS present with a constellation of phenotypic alterations involving most organs and organ systems. ID is present in all people with DS, albeit with variable severity. DS is also the most frequent genetic cause of Alzheimer's disease (AD), and ∼50% of those with DS will develop AD-related dementia. In the last few years, significant progress has been made in understanding the crucial genotype-phenotype relationships in DS, in identifying the alterations in molecular pathways leading to the various clinical conditions present in DS, and in preclinical evaluations of potential therapies to improve the overall health and well-being of individuals with DS. In June 2015, 230 scientists, advocates, patients, and family members met in Paris for the 1st International Conference of the Trisomy 21 Research Society. Here, we report some of the most relevant presentations that took place during the meeting

Characterization of PTZ-Induced Seizure Susceptibility in a Down Syndrome Mouse Model That Overexpresses CSTB

Down syndrome (DS) is a complex genetic syndrome characterized by intellectual disability, dysmorphism and variable additional physiological traits. Current research progress has begun to decipher the neural mechanisms underlying cognitive impairment, leading to new therapeutic perspectives. Pentylenetetrazol (PTZ) has recently been found to have positive effects on learning and memory capacities of a DS mouse model and is foreseen to treat DS patients. But PTZ is also known to be a convulsant drug at higher dose and DS persons are more prone to epileptic seizures than the general population. This raises concerns over what long-term effects of treatment might be in the DS population. The cause of increased propensity for epilepsy in the DS population and which Hsa21 gene(s) are implicated remain unknown. Among Hsa21 candidate genes in epilepsy, CSTB, coding for the cystein protease inhibitor cystatin B, is involved in progressive myoclonus epilepsy and ataxia in both mice and human. Thus we aim to evaluate the effect of an increase in Cstb gene dosage on spontaneous epileptic activity and susceptibility to PTZ-induced seizure. To this end we generated a new mouse model trisomic for Cstb by homologous recombination. We verified that increasing copy number of Cstb from Trisomy (Ts) to Tetrasomy (Tt) was driving overexpression of the gene in the brain, we checked transgenic animals for presence of locomotor activity and electroencephalogram (EEG) abnormalities characteristic of myoclonic epilepsy and we tested if those animals were prone to PTZ-induced seizure. Overall, the results of the analysis shows that an increase in Cstb does not induce any spontaneous epileptic activity and neither increase or decrease the propensity of Ts and Tt mice to myoclonic seizures suggesting that Ctsb dosage should not interfere with PTZ-treatment

Rapid Analysis of Saccharomyces cerevisiae Genome Rearrangements by Multiplex Ligation–Dependent Probe Amplification

Aneuploidy and gross chromosomal rearrangements (GCRs) can lead to genetic diseases and the development of cancer. We previously demonstrated that introduction of the repetitive retrotransposon Ty912 onto a nonessential chromosome arm of Saccharomyces cerevisiae led to increased genome instability predominantly due to increased rates of formation of monocentric nonreciprocal translocations. In this study, we adapted Multiplex Ligation–dependent Probe Amplification (MLPA) to analyze a large numbers of these GCRs. Using MLPA, we found that the distribution of translocations induced by the presence of Ty912 in a wild-type strain was nonrandom and that the majority of these translocations were mediated by only six translocation targets on four different chromosomes, even though there were 254 potential Ty-related translocation targets in the S. cerevisiae genome. While the majority of Ty912-mediated translocations resulted from RAD52-dependent recombination, we observed a number of nonreciprocal translocations mediated by RAD52-independent recombination between Ty1 elements. The formation of these RAD52-independent translocations did not require the Rad51 or Rad59 homologous pairing proteins or the Rad1–Rad10 endonuclease complex that processes branched DNAs during recombination. Finally, we found that defects in ASF1-RTT109–dependent acetylation of histone H3 lysine residue 56 (H3K56) resulted in increased accumulation of both GCRs and whole-chromosome duplications, and resulted in aneuploidy that tended to occur simultaneously with GCRs. Overall, we found that MLPA is a versatile technique for the rapid analysis of GCRs and can facilitate the genetic analysis of the pathways that prevent and promote GCRs and aneuploidy